Plasma thioredoxin levels during post-cardiac arrest syndrome: relationship with severity and outcome
1 Medical Intensive Care Unit, Cochin Hospital, Hôpitaux Universitaires Paris Centre, Assistance Publique des Hôpitaux de Paris, 27 rue du Faubourg Saint-Jacques, 75014 Paris, France
2 Université Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine, 15 rue de l'Ecole de Médecine, 75006 Paris, France
3 Department of Biochemistry, Cochin Hospital, Hôpitaux Universitaires Paris Centre, Assistance Publique des Hôpitaux de Paris, 27 rue du Faubourg Saint-Jacques, 75014 Paris, France
4 Unit of Critical Care, Respiratory Science, National Heart and Lung Institute Division, Faculty of Medicine, Imperial College London, Dovehouse Street, London SW3 6LY, UK
5 General Intensive Care Unit, Estaing Hospital, 1 place Lucie Aubrac, 63000 Clermont-Ferrand, France
6 Institut Cochin, INSERM U1016, CNRS UMR8104, 22 rue Méchain, 75014 Paris, France
7 INSERM U970, Paris Cardiovascular Research Center (PARCC), European Georges Pompidou Hospital, 56 rue Leblanc, 75015 Paris, France
Critical Care 2013, 17:R18 doi:10.1186/cc12492Published: 29 January 2013
Despite experimental evidence, clinical demonstration of acute state of oxidative stress and inflammation during post-cardiac arrest syndrome is lacking. Plasma level of thioredoxin (TRX), a redox-active protein induced under conditions of oxidative stress and inflammation, is increased in various critical care conditions. We determined plasma TRX concentrations after cardiac arrest and assessed relationships with severity and outcome.
Retrospective study of consecutive patients admitted to a single academic intensive care unit (ICU) for out-of-hospital cardiac arrest (between July 2006 and March 2008). Plasma levels of TRX were measured at admission, day (D) 1, 2 and 3.
Of 176 patients included, median TRX values measured in ICU survivors and non-survivors were, respectively: 22 ng/mL (7.8 to 77) vs. 72.4 (21.9 to 117.9) at admission (P < 0.001); 5.9 (3.5 to 25.5) vs. 23.2 (5.8 to 81.4) at D1 (P = 0.003); 10.8 (3.6 to 50.8) vs. 11.7 (4.5 to 66.4) at D2 (P = 0.22); and 16.7 (5.3 to 68.3) vs. 17 (4.3 to 62.9) at D3 (P = 0.96). Patients dying within 24 hours had significantly (P < 0.001) higher TRX levels (118.6 ng/mL (94.8 to 280)) than those who died after 24 hours or survived (50.8 (13.9 to 95.7) and 22 (7.8 to 77)). The area under the ROC curve to predict early death was 0.84 (0.76 to 0.91).
TRX levels on admission were significantly correlated with 'low-flow' duration (P = 0.003), sequential organ failure assessment (SOFA) score (P < 0.001), and blood lactate concentration (P < 0.001), but not with 'no-flow' duration or simplified acute physiology score (SAPS) II score. TRX levels and admission arterial pO2 correlated negatively (r = -0.17, P = 0.03). Finally, cardiac arrest with cardiac etiology exhibited lower levels of TRX than in cases of extra-cardiac cause (46 ng/mL (11 to 104) vs. 68 (42 to 137), P = 0.01).
Our data show for the first time that TRX levels were elevated early following cardiac arrest, suggestive of oxidative stress and inflammation occurring with this condition. Highest values were found in the most severe patients. TRX could be a useful tool for further exploration and comprehension of post-cardiac arrest syndrome.